Mechanotransduction from the extracellular matrix into the cell is primarily supervised by a transmembrane receptor, integrin, and a cytosolic protein, talin. Integrin binds ligands on the extracellular side, whereas talin couples integrin receptors to the actin cytoskeleton and later acts as a "force buffer". Talin and integrin together form a mechanosensitive signaling hub that regulates crucial cellular processes and pathways, including cell signaling and formation of focal adhesion complexes, which help cells to sense their mechanoenvironment and transduce the signal accordingly. Although both proteins function in tandem, most literature focuses on them individually. Here, we provide a focused review of the talin−integrin mechano-interactome network in light of its role in the process of mechanotransduction and its connection to diseases. While working under force, these proteins drive numerous biomolecular interactions and form adhesion complexes, which in turn control many physiological processes such as cell migration; thus, they are invariably associated with several diseases from leukocyte adhesion deficiency to cancer. Gaining insights into their role in the occurrence of these pathological disorders might lead us to establish treatment methods and therapeutic techniques.

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24Female-female nonsexual interference competition is rapidly emerging as a major fitness 25 determinant of biased sex-ratio groups with high female density. How do females overcome such 26 competition? We used adult flour beetle Tribolium castaneum to answer this question, where 27 females from female-biased groups suppressed each other's fecundity by secreting toxic quinones 28 from their stink glands, revealing a chemical-driven interference competition. The added natal 29 resource did not alleviate these fitness costs. Females also did not disperse more at high female-30 density. Hence, the competition was neither limited by the total resource availability nor the 31 inability to avoid chemical interference. Instead, protein sequestered via scavenging of nutrient-32 rich carcasses relaxed the female competition, by increasing their fecundity and reducing the 33 quinone content. Even infected carcasses were scavenged to extract fitness benefits, despite the 34 infection-risk. Finally, individual stink gland components triggered carcass-scavenging to increase 35 fecundity, indicating a potentially novel chemical feedback loop to reduce the competition. 36 37 38 39 40 41 42 43 44 45 46 3

Female-female nonsexual interference competition is rapidly emerging as a major fitness determinant of biased sex-ratio groups with high female density. How do females overcome such competition? We used adult flour beetle Tribolium castaneum to answer this question, where females from female-biased groups suppressed each other's fecundity by secreting toxic quinones from their stink glands, revealing a chemical-driven interference competition. The added natal resource did not alleviate these fitness costs. Females also did not disperse more at high female-density. Hence, the competition was neither limited by the total resource availability nor the inability to avoid chemical interference. Instead, protein sequestered via scavenging of nutrient-rich carcasses relaxed the female competition, by increasing their fecundity and reducing the quinone content.Even infected carcasses were scavenged to extract fitness benefits, despite the infection-risk. Finally, individual stink gland components triggered carcass-scavenging to increase fecundity, indicating a potentially novel chemical feedback loop to reduce the competition.